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James L. Mcgaugh - One of the best experts on this subject based on the ideXlab platform.
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Research Enhancement of Inhibitory Avoidance and Conditioned Taste Aversion Memory With Insular Cortex Infusions of 8-Br-cAMP:
2016Co-Authors: Involvement Of The Basolateral Amygdala, Marı́a I. Mir, James L. McgaughAbstract:There is considerable evidence that in rats, the insular cortex (IC) and amygdala are involved in the learning and memory of aversively motivated tasks. The present experiments examined the effects of 8-Br-cAMP, an analog of cAMP, and Oxotremorine, a muscarinic agonist, infused into the IC after inhibitory avoidance (IA) training and during the acquisition/consolidation of conditioned taste aversion (CTA). Posttraining infusion into the IC of 0.3 µg Oxotremorine and 1.25 µg 8-Br-cAMP enhanced IA retention. Infusions of 8-Br-cAMP, but not Oxotremorine, into the IC enhanced taste aversion. The experiments also examined whether noradrenergic activity in the basolateral amygdala (BLA) is critical in enabling the enhancement of CTA and IA memory induced by drug infusions administered into the IC. For both CTA and IA, ipsilateral infusions of -adrenergic antagonist propranolol administered into the BLA blocked the retention-enhancing effect of 8-Br-cAMP or Oxotremorine infused into the IC. These results indicate that the IC is involved in the consolidation of memory for both IA and CTA, and this effect requires intact noradrenergic activity into the BLA. These findings provide additional evidence that the BLA interacts with other brain regions, including sensory cortex, in modulating memory consolidation. Extensive evidence indicates that the insular cortex (IC) and amygdala are involved in the acquisition of aversively motivated tasks. Lesions or functional inactivation of either the IC or amyg
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enhancement of inhibitory avoidance and conditioned taste aversion memory with insular cortex infusions of 8 br camp involvement of the basolateral amygdala
Learning & Memory, 2004Co-Authors: Maria Isabel Miranda, James L. McgaughAbstract:There is considerable evidence that in rats, the insular cortex (IC) and amygdala are involved in the learning and memory of aversively motivated tasks. The present experiments examined the effects of 8-Br-cAMP, an analog of cAMP, and Oxotremorine, a muscarinic agonist, infused into the IC after inhibitory avoidance (IA) training and during the acquisition/consolidation of conditioned taste aversion (CTA). Posttraining infusion into the IC of 0.3 microg Oxotremorine and 1.25 microg 8-Br-cAMP enhanced IA retention. Infusions of 8-Br-cAMP, but not Oxotremorine, into the IC enhanced taste aversion. The experiments also examined whether noradrenergic activity in the basolateral amygdala (BLA) is critical in enabling the enhancement of CTA and IA memory induced by drug infusions administered into the IC. For both CTA and IA, ipsilateral infusions of beta-adrenergic antagonist propranolol administered into the BLA blocked the retention-enhancing effect of 8-Br-cAMP or Oxotremorine infused into the IC. These results indicate that the IC is involved in the consolidation of memory for both IA and CTA, and this effect requires intact noradrenergic activity into the BLA. These findings provide additional evidence that the BLA interacts with other brain regions, including sensory cortex, in modulating memory consolidation.
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posttraining intraamygdala infusions of Oxotremorine and propranolol modulate storage of memory for reductions in reward magnitude
Neurobiology of Learning and Memory, 1997Co-Authors: Juan A Salinas, Ines B Introinicollison, Carla Dalmaz, James L. McgaughAbstract:Abstract These experiments examined the effects of posttraining intraamygdala administration of the muscarinic agonist, Oxotremorine, and the β-noradrenergic antagonist, propranolol, on memory for reduction in reward magnitude. Male Sprague–Dawley rats (175–200 g) implanted with bilateral intraamygdala cannulae were food deprived (maintained at 80% of body weight) and trained to run a straight alley (six trials/day) for either ten 45-mg food pellets (high reward) or one 45-mg food pellet (low reward) for 10 days. In Experiment One, the animals in the high-reward group were then shifted to a one-pellet reward and immediately given intraamygdala infusions (0.5 μl/side) of either Oxotremorine (10 ng) or phosphate buffer. Shifted training continued for 4 more days and no further injections were given. Shifted animals given the buffer solution displayed an increase in runway latencies but returned to preshift latencies by the fifth day of shifted training. In contrast, animals given Oxotremorine exhibited increased latencies through the fifth day. In Experiment Two, rats were trained as in Experiment One but immediately following the shift received intraamygdala infusions of Oxotremorine (10 ng), propranolol (0.3 μg), both, or phosphate buffer. Shifted vehicle-injected rats returned to preshift performance by the fifth day of shifted training. Shifted propranolol rats returned to preshift latencies by the third day of shifted training. In contrast, the shifted Oxotremorine and the shifted Oxotremorine/propranolol rats displayed longer latencies than unshifted controls through 5 days of shifted training. The findings indicate that the muscarinic cholinergic and β-noradrenergic systems within the amygdala interact in regulating memory and support the view that noradrenergic influences are mediated through cholinergic activation.
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Stria Terminalis Lesions Attenuate Memory Enhancement Produced by Intracaudate Nucleus Injections of Oxotremorine
Neurobiology of learning and memory, 1996Co-Authors: Mark G. Packard, Ines B. Introini-collison, James L. McgaughAbstract:Abstract The present study examined the role of the stria terminalis in modulating the memory enhancement produced by posttraining intracaudate nucleus injection of Oxotremorine. Male Sprague–Dawley rats with either sham operations or bilateral lesions of the stria terminalis (ST) were trained on a one-trial inhibitory-avoidance task and received a unilateral posttraining intracaudate injection of either a buffer vehicle or the cholinergic agonist Oxotremorine (0.3 μg/0.5 μl) into a medial region of the caudate nucleus innervated by the ST. Intracaudate injection of Oxotremorine improved memory in sham-operated rats. Although ST lesions did not affect retention in rats given intracaudate injections of the buffer vehicle, ST lesions attenuated the memory enhancement produced by posttraining intracaudate injection of Oxotremorine. In view of anatomical evidence indicating that amygdalostriatal projections are nonreciprocol, the present findings suggest that amygdala output via the ST is essential for memory enhancement produced by intracaudate injection of Oxotremorine.
Hui Lin Pan - One of the best experts on this subject based on the ideXlab platform.
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dynamic control of glutamatergic synaptic input in the spinal cord by muscarinic receptor subtypes defined using knockout mice
Journal of Biological Chemistry, 2010Co-Authors: Shao Rui Chen, Hong Chen, Wei Xiu Yuan, Jurgen Wess, Hui Lin PanAbstract:Abstract Activation of muscarinic acetylcholine receptors (mAChRs) in the spinal cord inhibits pain transmission. At least three mAChR subtypes (M2, M3, and M4) are present in the spinal dorsal horn. However, it is not clear how each mAChR subtype contributes to the regulation of glutamatergic input to dorsal horn neurons. We recorded spontaneous excitatory postsynaptic currents (sEPSCs) from lamina II neurons in spinal cord slices from wild-type (WT) and mAChR subtype knock-out (KO) mice. The mAChR agonist Oxotremorine-M increased the frequency of glutamatergic sEPSCs in 68.2% neurons from WT mice and decreased the sEPSC frequency in 21.2% neurons. Oxotremorine-M also increased the sEPSC frequency in ∼50% neurons from M3-single KO and M1/M3 double-KO mice. In addition, the M3 antagonist J104129 did not block the stimulatory effect of Oxotremorine-M in the majority of neurons from WT mice. Strikingly, in M5-single KO mice, Oxotremorine-M increased sEPSCs in only 26.3% neurons, and J104129 abolished this effect. In M2/M4 double-KO mice, but not M2- or M4-single KO mice, Oxotremorine-M inhibited sEPSCs in significantly fewer neurons compared with WT mice, and blocking group II/III metabotropic glutamate receptors abolished this effect. The M2/M4 antagonist himbacine either attenuated the inhibitory effect of Oxotremorine-M or potentiated the stimulatory effect of Oxotremorine-M in WT mice. Our study demonstrates that activation of the M2 and M4 receptor subtypes inhibits synaptic glutamate release to dorsal horn neurons. M5 is the predominant receptor subtype that potentiates glutamatergic synaptic transmission in the spinal cord.
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Dynamic regulation of glycinergic input to spinal dorsal horn neurones by muscarinic receptor subtypes in rats
The Journal of Physiology, 2006Co-Authors: Xiu Li Wang, Hongmei Zhang, De Pei Li, Shao Rui Chen, Hui Lin PanAbstract:Activation of spinal muscarinic acetylcholine receptors (mAChRs) inhibits nociception. However, the cellular mechanisms of this action are not fully known. In this study, we determined the role of mAChR subtypes in regulation of synaptic glycine release in the spinal cord. Whole-cell voltage-clamp recordings were performed on lamina II neurones in the rat spinal cord slices. The mAChR agonist Oxotremorine-M significantly increased the frequency of glycinergic sIPSCs but not mIPSCs. Surprisingly, the effect of Oxotremorine-M on sIPSCs was largely attenuated at a higher concentration. On the other hand, 1-10 microm Oxotremorine-M dose-dependently increased the frequency of sIPSCs in rats pretreated with intrathecal pertussis toxin. Furthermore, Oxotremorine-M also dose-dependently increased the frequency of sIPSCs in the presence of himbacine (an M2/M4 mAChR antagonist) or AF-DX116 (an M2 mAChR antagonist). The M3 mAChR antagonist 4-DAMP abolished the stimulatory effect of Oxotremorine-M on sIPSCs. Interestingly, the GABA(B) receptor antagonist CGP55845 potentiated the stimulatory effect of Oxotremorine-M on sIPSCs. In the presence of CGP55845, both himbacine and AF-DX116 similarly reduced the potentiating effect of Oxotremorine-M on sIPSCs. Collectively, these data suggest that the M3 subtype is present on the somatodendritic site of glycinergic neurones and is mainly responsible for muscarinic potentiation of glycinergic input to spinal dorsal horn neurones. Concurrent stimulation of mAChRs on adjacent GABAergic interneurones attenuates synaptic glycine release through presynaptic GABA(B) receptors on glycinergic interneurones. This study illustrates a complex dynamic interaction between GABAergic and glycinergic synapses in the spinal cord dorsal horn.
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m2 m3 and m4 receptor subtypes contribute to muscarinic potentiation of gabaergic inputs to spinal dorsal horn neurons
Journal of Pharmacology and Experimental Therapeutics, 2005Co-Authors: Hongmei Zhang, Shao Rui Chen, Hui Lin PanAbstract:The spinal cholinergic system and muscarinic receptors are important for regulation of nociception. Activation of spinal muscarinic receptors produces analgesia and inhibits dorsal horn neurons through potentiation of GABAergic inputs. To determine the role of receptor subtypes in the muscarinic agonist-induced synaptic GABA release, spontaneous inhibitory postsynaptic currents (sIPSCs) were recorded in lamina II neurons using whole-cell voltage-clamp recordings in rat spinal cord slices. The muscarinic receptor agonist Oxotremorine-M dose-dependently (1–10 μM) increased GABAergic sIPSCs but not miniature IPSCs. The potentiating effect of Oxotremorine-M on sIPSCs was completely blocked by atropine. In rats pretreated with intrathecal pertussis toxin to inactive inhibitory G i/o proteins, 3 μM Oxotremorine-M had no significant effect on sIPSCs in 31 of 55 (56%) neurons tested. In the remaining 24 (44%) neurons in pertussis toxin-treated rats, Oxotremorine-M caused a small increase in sIPSCs, and this effect was completely abolished by subsequent application of 25 nM 4-diphenylacetoxy- N -methylpiperidine methiodide (4-DAMP), a relatively selective M3 subtype antagonist. Furthermore, himbacine (1 μM), a relatively specific antagonist for M2 and M4 subtypes, produced a large reduction in the stimulatory effect of Oxotremorine-M on sIPSCs, and the remaining effect was abolished by 4-DAMP. Additionally, the M4 receptor antagonist MT-3 toxin (100 nM) significantly attenuated the effect of Oxotremorine-M on sIPSCs. Collectively, these data suggest that M2 and M4 receptor subtypes play a predominant role in muscarinic potentiation of synaptic GABA release in the spinal cord. The M3 subtype also contributes to increased GABAergic tone in spinal dorsal horn by muscarinic agonists.
E Leung - One of the best experts on this subject based on the ideXlab platform.
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functional interactions between muscarinic m2 receptors and 5 hydroxytryptamine 5 ht 4 receptors and β adrenoceptors in isolated oesophageal muscularis mucosae of the rat
British Journal of Pharmacology, 1996Co-Authors: Richard M Eglen, B Peelle, M T Pulidorios, E LeungAbstract:1. Relaxations of isolated oesophageal muscularis mucosae of rat are mediated by 5-hydroxytryptamine (5-HT), acting at 5-HT4 receptors, and isoprenaline, principally acting via beta 3-adrenoceptors. The aim of this study was to investigate the hypothesis that muscarinic M2 receptors, also present in this tissue, functionally oppose 5-HT and beta-adrenoceptor-relaxant effects in this preparation. 2. Contractions of rat oesophageal muscularis mucosae were induced, in a concentration-dependent manner, by the muscarinic receptor agonist, Oxotremorine M (pEC50 = 6.7 +/- 0.1). The contractile responses to Oxotremorine M were surmountably antagonized by the following compounds, (pKB values in parentheses): atropine (9.1 +/- 0.2), 4-DAMP (4-diphenylacetoxy-N-methyl piperidine methiodide, 8.7 +/- 0.1), p-F-HHSiD (para-fluoro-hexa-hydro-siladifenidol, 7.5 +/- 0.1), zamifenacin (8.6 +/- 0.3), himbacine (7.2 +/- 0.2), pirenzepine (6.8 +/- 0.3) and methoctramine (6.2 +/- 0.2). These data are consistent with a role for muscarinic M3 receptors mediating contractions to Oxotremorine M. The contractile response was associated with a low receptor reserve, since the responses were shifted to the right and virtually abolished by the alkylating agent, 4-DAMP mustard (4-diphenylacetoxy-N-(2-chloroethyl) piperidine, 40 nM; 60 min equilibration). 3. In tissues precontracted with U46619 (0.7 microM; approx. EC90), isoprenaline (pEC50 = 8.0 +/- 0.1) and 5-HT (pEC50 = 7.5 +/- 0.2) induced concentration-dependent relaxations. The isoprenaline potency was slightly, but significantly, different in tissues precontracted with Oxotremorine M (isoprenaline, pEC50 = 7.4 +/- 0.2). In contrast, the potency of 5-HT (pEC50 = 7.5 +/- 0.2), in tissues that were precontracted with 1 microM (EC90) Oxotremorine M, was identical. When these experiments were repeated in the presence of the muscarinic M2 receptor antagonist, methoctramine (1 microM), there was no effect on the relaxant potencies to either 5-HT or isoprenaline. Collectively, these data suggest that muscarinic M2 receptors do not, under these conditions, modulate relaxant potencies to either 5-HT or isoprenaline. 4. In a second protocol, tissues were pre-contracted with U46619 (0.7 microM) and relaxed with either 5-HT (0.1 microM) or isoprenaline (0.1 microM). In these tissues (in which the muscarinic M3 receptor population was extensively depleted by alkylation), Oxotremorine M caused concentration-dependent re-contractions (i.e. reversal of relaxations). In tissues relaxed with 5-HT, the potency of oxtremorine M was 5.9 +/- 0.2, while in tissues relaxed with isoprenaline, the potency (pEC50) = 5.6 +/- 0.3. These re-contractions were antagonized, in a surmountable fashion, by methoctramine (1 microM; pKB = 7.6 +/- 0.1). Similar observations were seen when relaxations were induced by isoprenaline (1 microM; pKB = 7.5 +/- 0.2). Under these conditions, therefore, the pKB values are consistent with activation of muscarinic M2 receptors, and inconsistent with activation of M3 receptors. 5. It is concluded that in isolated oesophageal muscularis mucosae of rat, muscarinic M3 receptors mediate direct contractions and are associated with a low receptor reserve. When this population is depleted, and the tissues relaxed via activation of receptors that augment adenylyl cyclase activity, a functional role for muscarinic M2 receptors is revealed.
Frederick J Ehlert - One of the best experts on this subject based on the ideXlab platform.
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pertussis toxin blocks m2 muscarinic receptor mediated effects on contraction and cyclic amp in the guinea pig ileum but not m3 mediated contractions and phosphoinositide hydrolysis
Journal of Pharmacology and Experimental Therapeutics, 1994Co-Authors: Elizabeth A Thomas, Frederick J EhlertAbstract:The effects of pertussis toxin on muscarinic receptor-induced contractions of the isolated guinea pig ileum were investigated. In control tissues, isoproterenol (1 microM) only slightly inhibited contractions in response to Oxotremorine-M; however, in pertussis toxin-treated tissues, isoproterenol exhibited an enhanced inhibition of the concentration-effect curve. Under basal conditions, pertussis toxin had no dampening effect on Oxotremorine-M-induced contractions. When ilea were precontracted with histamine (1 microM) and then relaxed back to base line using forskolin (10 microM) before contractile responses to Oxotremorine-M were measured, pertussis toxin shifted the concentration-effect curve to Oxotremorine-M by a 6.1-fold increase in the EC50 value. Ilea were then incubated with [N-(2-chloroethyl)-4-piperidinyl diphenylacetate] (40 nM; 1 hr) in the presence of [[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5,11- dihydro-6H-pyrido[2,3b][1,4]benzodiazepine-6-one (1 microM) to selectively inactivate the M3 muscarinic receptors. Under these conditions, pertussis toxin blocked the concentration-effect curve to Oxotremorine-M by a 30-fold increase in the EC50 value. Prior treatment of guinea pigs in vivo with pertussis toxin diminished the labeling of a 41-kDa protein in membranes suspensions of the longitudinal muscle incubated with [32P]nicotinamide adenine dinucleotide] and pertussis toxin. This ADP-ribosylation caused a functional uncoupling of the G protein from its receptor as indicated by radioligand-binding studies and second messenger assays. Our results verify that the M2 muscarinic acetylcholine receptor, like the M3 receptor, can elicit contractions of the guinea pig ileum and that the mechanism of this action involves inhibition of adenylate cyclase.
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specific inhibition of isoproterenol stimulated cyclic amp accumulation by m2 muscarinic receptors in rat intestinal smooth muscle
Journal of Pharmacology and Experimental Therapeutics, 1992Co-Authors: Michael T Griffin, Frederick J EhlertAbstract:The ability of Oxotremorine-M to inhibit cyclic AMP accumulation in the presence of a variety of adenylate cyclase activators was studied in slices from the longitudinal muscle of the rat ileum. Oxotremorine-M was found to inhibit forskolin- and isoproterenol-stimulated cyclic AMP accumulation maximally by 17 and 32%, respectively, but not the stimulation due to other activators of adenylate cyclase. Inhibition of cyclic AMP accumulation by Oxotremorine-M was unaffected by tetrodotoxin and was completely reversed by atropine. AF-DX 116 (11[[2-[(diethylamino)methyl]-1- piperidynyl]acetyl]-5,11-dihydro-6H-pyrido[2,3- b][1,4]benzodiazepine-6-one) an M2-selective antagonist, shifted the Oxotremorine-M dose-response curve to the right with a dissociation constant (KB) of 0.20 microM, consistent with the dissociation constants for binding at the M2 muscarinic receptor site (KD = 0.092 microM) and inhibition of adenylate cyclase activity (KB = 0.13 microM). Hexahydrosiladifenidol, an M3-selective antagonist, shifted the Oxotremorine-M dose-response curve to the right with a dissociation constant of 0.67 microM, again consistent with the dissociation constant for binding at the M2 site (KD = 0.83 microM). The agreement between the estimates of the dissociation constants of muscarinic antagonists for binding and for inhibition of cyclic AMP accumulation suggest that Oxotremorine-M inhibition of isoproterenol-stimulated cyclic AMP accumulation in slices of rat intestinal smooth muscle is mediated by the M2 receptor.
Jean-rené Cazalets - One of the best experts on this subject based on the ideXlab platform.
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Cholinergic-mediated coordination of rhythmic sympathetic and motor activities in the newborn rat spinal cord
PLoS Biology, 2018Co-Authors: Mélissa Sourioux, Sandrine Bertrand, Jean-rené CazaletsAbstract:Here, we investigated intrinsic spinal cord mechanisms underlying the physiological requirement for autonomic and somatic motor system coupling. Using an in vitro spinal cord preparation from newborn rat, we demonstrate that the specific activation of muscarinic cholinergic receptors (mAchRs) (with Oxotremorine) triggers a slow burst rhythm in thoracic spinal segments, thereby revealing a rhythmogenic capability in this cord region. Whereas axial motoneurons (MNs) were rhythmically activated during both locomotor activity and Oxotremorine-induced bursting, intermediolateral sympathetic preganglionic neurons (IML SPNs) exhibited rhythmicity solely in the presence of Oxotremorine. This somato-sympathetic synaptic drive shared by MNs and IML SPNs could both merge with and modulate the locomotor synaptic drive produced by the lumbar motor networks. This study thus sheds new light on the coupling between somatic and sympathetic systems and suggests that an intraspinal network that may be conditionally activated under propriospinal cholinergic control constitutes at least part of the synchronizing mechanism.
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Inhibitory component of the somato-sympathetic drive induced by Oxotremorine.
2018Co-Authors: Mélissa Sourioux, Sandrine S. Bertrand, Jean-rené CazaletsAbstract:(A) Recordings from a right thoracic (rT13) ventral root and a rT10 MN at two different membrane potentials during the bath-application of 10 μM Oxotremorine (A1). Note the reversed inhibitory synaptic drive at −92 mV compared to −60 mV. Recordings from an rT10 ventral root and a rT9 IML under Oxotremorine (A2). (B) Same MN as in A1 in the presence of Oxotremorine and the GABAergic and glycinergic receptor antagonists, gabazine and strychnine (1 μM each), respectively. The gray panels in each case present an enlarged section of the intracellular recording to highlight the inhibitory postsynaptic potentials received by the MN and IML in the Oxotremorine condition and their disappearance during the disinhibited rhythm with large spike bursts induced by Oxotremorine in the presence of the strychnine/gabazine cocktail. Vertical calibration bars: 5 mV. IML, intermediolateral neuron; l, left; MN, motoneuron; r, right; T, thoracic.
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Dose-dependent effects of Oxotremorine.
2018Co-Authors: Mélissa Sourioux, Sandrine S. Bertrand, Jean-rené CazaletsAbstract:(A) Recordings from right thoracic 11 and left thoracic 12 (rT11, lT12) ventral roots in the presence of increasing concentrations of Oxotremorine bath-applied to the same whole thoracolumbar cord preparation (A1–A5). (B, C) Box plots of burst cycle period (B) and normalized amplitude (C) at different Oxotremorine concentrations. Motor burst amplitudes were normalized to the mean burst amplitude computed in the presence of 0.5 μM Oxotremorine in each experiment. (D) Polar graphs of the right and left alternation of thoracic motor bursts (Pop ϕ rTh-lTh) computed under increasing concentrations of Oxotremorine (Oxo). 0, in phase; 0.5, antiphase. The direction and length of vectors (blue lines) indicate phase means and dispersions, respectively. Each dot on polar graphs represents one experiment. *p < 0.05. l, left; n, number of preparations; Oxo, Oxotremorine; Pop, population; Pop ϕ rTh-lTh, right and left alternation of thoracic motor bursts; r, right; T, thoracic.
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Oxotremorine-induced synaptic merging of slow and fast motor rhythms.
2018Co-Authors: Mélissa Sourioux, Sandrine S. Bertrand, Jean-rené CazaletsAbstract:Recordings from a left lumbar 2 (lL2) ventral root and a right thoracic (rT10) MN during bath-application to the whole thoracolumbar spinal cord of NMDA/5-HT alone (A), 10 μM Oxotremorine alone (B), and NMDA/5-HT plus Oxotremorine (C). The conjoint presence of Oxotremorine + NMDA/5-HT produced a merging of the slow and fast motor rhythms. l, left; L, lumbar; MN, motoneuron; NMDA, N-methyl-D-aspartate; T, thoracic; 5-HT, serotonin.
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Glutamatergic interneurons are involved in the somato-sympathetic synaptic drive induced by Oxotremorine.
2018Co-Authors: Mélissa Sourioux, Sandrine S. Bertrand, Jean-rené CazaletsAbstract:(A) Recordings from left lumbar 2 (lL2), right L2 (rL2), and right thoracic (rT8) ventral roots and an rT8 MN in the presence of Oxotremorine alone (A1) or in combination with the NMDA and non-NMDA receptor antagonists, DNQX and AP5, respectively (A2). (B) A different preparation with lumbar and thoracic (lL2, rL2, rT5) ventral root recordings together with an intracellularly recorded rT5 IML SPN under Oxotremorine alone (B1), then Oxotremorine plus the glutamatergic receptor antagonists (B2). AP5, 2-amino-5-phosphonovalerate; DNQX, 6, 7-dinitroquinoxaline-2,3-dione; IML SPN, intermediolateral sympathetic preganglionic neuron; l, left; L, lumbar; MN, motoneuron; NMDA, N-methyl-D-aspartate; r, right; T, thoracic.
